Headaches Alan Chan MD 12 16 prevalence Tension

Headaches Alan Chan, MD

• • 12 -16 % prevalence Tension most common Cluster HA men > women All other types women > men • International Headache Society (IHS) classification updated in 2004 • HA, cranial neuralgia, facial pain syndromes.

HA • Migraine – 2/3 unilat, 1/3 bilat or global; crescendo pattern, pulsating; 4 -72 hr; +/aura • Tension – bilat, pressure/tightness variable; indeterminate length • Cluster – unilat, quick and explosive; patient active; < 3 hr; ipsilat facial symptoms – tearing, nasal congestion, Horner’s, rarely focal neuro symptoms

Ddx – less common • • • Paroxysmal hemicrania Idiopathic stabbing headache Cold-stimulus headache Benign cough headache Benign exertional headache Headache associated with sexual activity

Other HA • Secondary HA – associated with trauma, vascular disorder, nonvascular intracranial disorder, substance use or withdrawal, infection, metabolic disorder, other facial or cranial structures

Get some hx • Triggers – Diet, stress, hormones, sensory stimuli, change in habit or environment • Important questions in history – frequency of severe headache (difficult to function) – frequency of milder HA – frequency of taking analgesics – change in HA

Image if… • recent significant change in pattern, frequency, or severity • worsening despite therapy • focal neurological signs/symptoms • HA with exertion, cough, or sexual activity • Orbital bruit • Onset after age 40

Migraine • episodes of severe HA typically with nausea +/- photo/phonophobia

Pathophysiology - NOT vascular dilatation of blood vessels • Primary neuro dysfunction leading to premonitory symptoms, aura, HA, and postdrome • Central process either brainstem or cortical spreading depression – causes aura, activates trigeminal nerve afferent fibers, alter blood brain barrier (BBB) permeability

• trigeminovascular system – activity leading to stimulation releases vasoactive neuropeptides of substance P, calcitonin gene-related protein (CGRP, which is a profound endogenous vasodilator), neurokinin A, activation of arachadonic acid cascade • sensitization – neurons get progressive more sensitive to nociceptive and non-nociceptive stimulation

More… • Genetics – approx 3 x risk in patients with relatives who had migraines. Non-Mendelian pattern of inheritance • Prodrome – 60% of people with migraine; can occur 1 -2 days prior to HA onset. Includes depression, irritability, constipation, euphoria, food craving, increased yawning. • Aura – 25%; typically visual like scotoma, but can be sensory, verbal, or motor • Headache – typically unilateral and throb/pulse • Postdrome – exhausted, sudden head mvt causes pain

Diagnosis – without aura • Headache attacks last 4 to 72 hours • Headache has at least two of the following characteristics: unilateral location; pulsating quality; moderate or severe intensity; aggravation by routine physical activity • During headache at least one of the following occurs: nausea and/or vomiting; photophobia and phonophobia • At least five attacks occur fulfilling the above criteria • History, physical examination, and neurologic examination do not suggest any underlying organic disease

Aura • At least one of the following characteristics without motor weakness: – Fully reversible visual symptoms including positive features (eg, flickering lights, spots, or lines) and/or negative features (eg, loss of vision) – Fully reversible sensory symptoms including positive features (eg, pins and needles) and/or negative features (eg, numbness) – Fully reversible dysphasic speech disturbance • Aura has at least two of the following characteristics: – Homonymous visual symptoms and/or unilateral sensory symptoms – At least one aura symptom develops gradually over ≥ 5 minutes and/or different aura symptoms occur in succession over ≥ 5 minutes – Each symptom lasts ≥ 5 and ≤ 60 minutes

Complications • Chronic (>15 days a month for > 3 months in absence of drug overuse) • Status migrainosus - > 72 hr and debilitating • Persistent aura without infarction – aura > 1 wk • Migrainous infarction – deficit > 1 hr and positive imaging • Migraine triggered seizure

Acute therapy • NSAIDs, combo Tylenol/ASA/caffeine, triptans, ergots like dihydroergotamine (DHE), opioids (but weak evidence only for butorphanol nasal and worry about abuse and transformation into chronic daily HA), IV metoclopramide.

Preventive Tx – can take as long as 2 -3 months to see benefit. • Treat if >2 a month that last > 3 days of disability, contraindication to acute tx, > 2 times a week use of acute tx, presence of uncommon conditions • Nonselective beta blockers – propranolol studied the most • TCA (better for mixed migraine and tension HA) like amitriptylline as others not studies as much; limited evidence for fluoxetine • Anticonvulsants - divalproex sodium and sodium valproate, limited evidence for gabapentin • NSAIDs – only naproxen with modest effect, but overuse syndrome • Serotonergic agent – ergot like DHE

• Keep a headache diary of related activities and triggers!

Cluster Headache • trigeminal autonomic cephalalgias, which are short, unilat, severe with autonomic symptoms (ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, nasal congestion)

• • Prevalence - <1 % Dx – very typical. < 3 hrs Tx – Acute – O 2, triptans, octreotide, lidocaine (intranasal), ergot • Preventive – CCB like verapamil, glucocorticoids, lithium (limited evidence), topiramate • Others less used – pizotifen (anti serotonergic), valproic acid, capsaicin, ergot, melatonin, indomethacin, triptans

Tension type headache (TTH) • Most common • Types – infrequent episodic (< 1 /month), freq episodic (1 -14/month), and chronic (> 15 days a month) • PP – multifactorial. Normally innocuous stimuli are interpreted as pain in the dorsal horn neurons. Some genetic role. Women slightly more than men. Blacks less than whites.

Dx – usually non descript! • TTH is characterized by having at least two of the following four features: • The location of the pain is bilateral in either the head or neck • The quality of the pain is steady (eg, pressing or tightening) and nonthrobbing • The intensity of the pain is mild to moderate • There is no aggravation of the headache by normal physical activity

• In addition to these criteria, there must be at least 10 headache episodes fulfilling all other ICHD-2 criteria, which include the following: • The duration of pain is between 30 minutes to 7 days • The headache is not attributable to another disorder

Tx • Acute – early tx, some may require a higher dose, avoid overuse, consider preventive. Tylenol, NSAIDs, ASA. Add some caffeine, but may get side effects. Butalbital and opioids generally not recommended. • Preventive – TCAs, Serotonin-NE reuptake inhibitors like venlafaxine, behavioral like CBT, relaxation, biofeedback

References • Uptodate. com • Snow V, Weiss K, Wall EM, et al. Pharmacologic Management of Acute Attacks of Migraine and Prevention of Migraine Headache. Ann Int Med. 2002. 137(10): 840 -849. • Clinch CR. Evaluation of Acute Headaches in Adults. Am Fam Physician. 2001. 63(4): 685693. • Tepper SJ, Spears RC. Acute Treatment of Migraine. Neuro Clinics 2009. 27(2): 417 -427